Determinants of Cardiac Output

Define the components and determinants of cardiac output

Cardiac output a function of Heart Rate (HR) and Stroke Volume (SV):
.

  • Heart rate is fairly intuitive
  • Stroke volume is defined as the difference between ESV and EDV, i.e.
    Stroke volume is a function of three factors:
    • Preload
    • Afterload
    • Contractility
  • Preload and afterload have almost as many definitions as there are textbooks
  • For the purpose of the exam, it's good to have both a laboratory and a clinical definition
  • These definitions are those which have appeared in old examiner reports, or given to me by cardiac anaesthetists

Preload

Preload is defined as the myocardial sarcomere length just prior to contraction.

  • As this is not measurable without removing the heart and cutting it into tiny pieces, clinically it is usually approximated by EDV or, less appropriately, by EDP

Determinants of Preload

Preload is a function of:

  • Venous Return
    • Intrathoracic Pressure
    • MSFP
      • Venous compliance
        A decrease in venous compliance will increase LVEDP.
      • Volume state
  • Ventricular compliance
    Reduced in diastolic dysfunction.
  • Pericardial compliance
  • Valvular disease
    • AV valve disease will impair preload
    • Semilunar valve disease will increase preload
  • Atrial kick
  • Wall thickness
    Increased ventricular wall thickness decreases preload.
    • HOCM/Hypertrophy

Preload and the Respiratory Cycle

  • Negative intrathoracic pressure causes RAP and PCWP to fall
  • This increases RA filling, so and RVEDP and RVEDV increase relative to the pleural pressure (though absolute pressure is still low)
  • LV effects are more variable
    Negative intrapleural pressures:
    • Increase LV transmural pressure
      This impairs ejection.
    • Cause bowing of the interventricular septum into the LV
      This reduces LVEDV.

Frank-Starling Mechanism

  • The Frank-Starling Law of the Heart states that the strength of cardiac contraction is dependent on initial fibre length
  • At a cellular level, additional stretch increases:
    • The number of myofilament crossbridges that can interact
    • Myofilament Ca2+ sensitivity
  • This law is represented by the ventricular function curve
    Plot of preload against stroke volume (or cardiac output, assuming a constant heart rate).
    • Right shift of the curve demonstrates negative inotropy
    • Left shift of the curve demonstrates positive inotropy

The failing ventricle:

  • In cardiac failure, the ventricle becomes overstretched
    This reduces the number of overlapping crossbridges, reducing contractility.
  • This is limited in the acute setting by constriction of the pericardium, which prevents excessive ventricular dilation

Afterload

Afterload is the sum of forces, both elastic and kinetic, opposing ventricular ejection

  • This definition is a bit wordy but avoids using the words "resistance" and "impedance", which are strictly defined in physics (and crudely applied in medicine), and may be leapt on by the cruel examiner

Determinants of Afterload

Afterload is equal to ventricular wall stress, which is given by the equation:

, where:

  • is ventricular wall stress
  • is ventricular transmural pressure
  • is ventricular chamber radius
  • is ventricular wall thickness

Each of these factors are in turn influenced by:

  • Ventricular transmural systolic pressure
    Transmural pressure is the difference between intrathoracic pressure and the ventricular cavity pressure during ejection.
    • Intrathoracic Pressure
      Negative intrathoracic pressure will increase afterload, as the ventricle has to generate a greater change in pressure to achieve ejection.
      • PEEP reduces LV afterload
      • Negative-pressure ventilation with a high work of breathing increases afterload
        This is why APO deteriorates - increased work of breathing increases LV afterload and worsens LV failure, increased pulmonary oedema, causing increased work of breathing...

    • Ventricular cavity pressure
      To facilitate ejection, the ventricle must overcome:
      • Outflow tract impedance
        • Valvular disease
          • e.g. aortic stenosis
        • HOCM
      • Systemic arterial impedance
        Determined by resistance (SVR), inertia, and compliance:
        • Determinants of resistance are stated in the Poiseuille Equation:
          , where:
          • η = Viscosity
            Affected by haematocrit (e.g. increased in polycythaemia)
          • l = Vessel length
            Essentially fixed.
          • r = Vessel radius
            • Greatest determinant
            • Function of degree of vasoconstriction of resistance vessels
        • Inertia
          • Given by the mass of blood in the column
          • Affected by heart rate
        • Arterial compliance
          Decreased arterial compliance increases afterload.
          • During ejection, the aorta and large arteries distend, reducing peak systolic pressure (impedance to further ejection)
            • Decreased arterial compliance increases the change in pressure for any given volume, increasing afterload during ejection
            • Decreased arterial compliance increases the speed of propagation of reflected pressures waves returning to the aortic root
              • Wave arrival in diastole augments coronary blood flow
              • Wave arrival during systole further increases afterload
          • In diastole the arteries recoil and blood pressure and flow are maintained - the Windkessel effect.
  • Ventricular chamber radius
    • End-Diastolic Volume
      Increased EDV increases ventricular radius and therefore wall tension.
  • Myocardial wall thickness
    Increasing wall thickness (seen clinically as ventricular hypertrophy) decreases afterload by sharing wall tension (the product of pressure and radius) between a larger number of sarcomeres.

Contractility

Contractility describes the factors other than heart rate, preload, and afterload that are responsible for for changes in myocardial performance.

Determinants of Contractility

Contractility is primarily dependent on intracellular Ca2+. Determinants include:

  • Drugs
  • Disease
    • Ischaemia
      Reduced ATP production secondary to hypoxia, which impairs sarcoplasmic reticulum Ca2+ function. Further exacerbated by intracellular acidosis from anaerobic metabolism.
    • Heart Failure
      Impaired contractility reserve, i.e. minimal increase in contractility with sympathetic stimulation.
      • Reduced peak Ca2+ and sarcoplasmic reticulum uptake of Ca2+
  • Autonomic Tone
  • Bowditch Effect
    Contractility improves at faster heart rates. This is because the myocardium does not have time to remove calcium, so it accumulates intracellularly.
  • Anrep Effect
    Contractility increases as afterload increases.

Measuring Contractility

  • As with the other determinants of cardiac output, there has been some difficulty in developing measurable indicies for contractility
  • All measures of contractility are affected by preload or afterload to some extent
  • dP/dtmax ()
    The rate of rise of LVP, assuming a constant preload and afterload
    • This index is preload dependent but afterload independent
    • Typically, the dP/dtmax in isovolumetric ventricular contraction is used
    • A greater rate of rise indicates a more forceful contraction
    • Measurement requires LV catheterisastion
  • End-Systolic Pressure-Volume Relationship
    • Uses the ventricular Pressure-Volume Relationship
    • Line plotted at the tangent to the curve from the end-systolic point (when isovolumetric ventricular relaxation begins)
      • The steeper the gradient the greater the contractility
  • Ejection Fraction
    Most common method used clinically is ejection fraction:

Footnotes

  • The use of wall stress for preload and afterload comes from the Cardiovascular Haemodynamics text, but is not used in the CICM texts

  • This site has a nice overview of wall tension, and the relationship of pressure to radius

  • This article discusses the wall stress definition for preload and afterload

  • Changes with ventilation are described with pretty graphs here


References

  1. Brandis K. The Physiology Viva: Questions & Answers. 2003.
  2. Deranged Physiology - Haemodynamic changes during mechanical ventilation
  3. Anwaruddin S, Martin JM, Stephens JC, Askari AT. Cardiovascular hemodynamics: an introductory guide, contemporary cardiology. New York: Springer; 2013. p. 29–51.
  4. Norton JM. Toward Consistent Definitions for Preload and Afterload. Advances in Physiology Education Mar 2001, 25 (1) 53-61.
  5. ANZCA July/September 2006
Last updated 2018-07-14

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